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10.1084/jem.20150537

http://scihub22266oqcxt.onion/10.1084/jem.20150537
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suck abstract from ncbi


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pmid27114609
      J+Exp+Med 2016 ; 213 (5 ): 751-69
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  • Continuous inhibitory signaling by both SHP-1 and SHIP-1 pathways is required to maintain unresponsiveness of anergic B cells #MMPMID27114609
  • Getahun A ; Beavers NA ; Larson SR ; Shlomchik MJ ; Cambier JC
  • J Exp Med 2016[May]; 213 (5 ): 751-69 PMID27114609 show ga
  • Many autoreactive B cells persist in the periphery in a state of unresponsiveness called anergy. This unresponsiveness is rapidly reversible, requiring continuous BCR interaction with self-antigen and resultant regulatory signaling for its maintenance. Using adoptive transfer of anergic B cells with subsequent acute induction of gene deletion or expression, we demonstrate that the continuous activities of independent inhibitory signaling pathways involving the tyrosine phosphatase SHP-1 and the inositol phosphatase SHIP-1 are required to maintain anergy. Acute breach of anergy by compromise of either of these pathways leads to rapid cell activation, proliferation, and generation of short-lived plasma cells that reside in extrafollicular foci. Results are consistent with predicted/observed reduction in the Lyn-SHIP-1-PTEN-SHP-1 axis function in B cells from systemic lupus erythematosus patients.
  • |*Clonal Anergy [MESH]
  • |Animals [MESH]
  • |B-Lymphocytes/*immunology/pathology [MESH]
  • |Humans [MESH]
  • |Lupus Erythematosus, Systemic/genetics/*immunology/pathology [MESH]
  • |Mice [MESH]
  • |Mice, Transgenic [MESH]
  • |PTEN Phosphohydrolase/genetics/immunology [MESH]
  • |Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases/genetics/*immunology [MESH]
  • |Protein Tyrosine Phosphatase, Non-Receptor Type 6/genetics/*immunology [MESH]
  • |Signal Transduction/genetics/*immunology [MESH]


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